Dataset Information

Whole Genome Metabolism - Chlorobaculum parvum (strain NCIB 8327)

ABSTRACT:

Whole Genome Metabolism of "Chlorobaculum parvum (strain NCIB 8327)"

This is a whole genome metabolism model of Chlorobaculum parvum (strain NCIB 8327).

This model has been automatically generated by the SuBliMinaL Toolbox and libAnnotationSBML using information coming from from KEGG (release 66, April 2013, accessed via the resource's web services interface) and, where relevant, augmented with metabolic pathway information extracted from MetaCyc (version 17.0, March 2013).

This model has been produced by the path2models project and is currently hosted on BioModels Database and identified by: BMID000000141912 .

Other models with the same genus include BMID000000022042 BMID000000022043 BMID000000022044 BMID000000022045 BMID000000022046 BMID000000022047 BMID000000022048 BMID000000022049 BMID000000022050 BMID000000022051 BMID000000022052 BMID000000022053 BMID000000022054 BMID000000022055 BMID000000118752 BMID000000118753 BMID000000118754 BMID000000118755 BMID000000118756 BMID000000118757 BMID000000118758 BMID000000118759 BMID000000118760 BMID000000118761 BMID000000118762 BMID000000118763 BMID000000118764 BMID000000118765 BMID000000118766 BMID000000118767 BMID000000118768 BMID000000118769 BMID000000118770 BMID000000118771 BMID000000118772 BMID000000118773 BMID000000118774 BMID000000118775 BMID000000118776 BMID000000118777 BMID000000118778 BMID000000118779 BMID000000118780 BMID000000118781 BMID000000118782 BMID000000118783 BMID000000118784 BMID000000118785 BMID000000118786 BMID000000118787 BMID000000118788 BMID000000118789 BMID000000118790 BMID000000118791 BMID000000118792 BMID000000118793 BMID000000118794 BMID000000118795 BMID000000118796 BMID000000118797 BMID000000118798 BMID000000118799 BMID000000118800 BMID000000118801 BMID000000118802 BMID000000118803 BMID000000118804 BMID000000118805 BMID000000118806 BMID000000118807 BMID000000118808 BMID000000118809 BMID000000118810 BMID000000118811 BMID000000118812 BMID000000118813 BMID000000118814 BMID000000118815 BMID000000118816 BMID000000118817 BMID000000118818 BMID000000118819 BMID000000118820 BMID000000118821 BMID000000118822 BMID000000118823 BMID000000118824 .

To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

SUBMITTER: Path2Models project

PROVIDER: BMID000000141912 | biostudies-other |

SECONDARY ACCESSION(S): 24180668

REPOSITORIES: biostudies-other

ACCESS DATA

Publications

Path2Models: large-scale generation of computational models from biochemical pathway maps.

Büchel Finja F Rodriguez Nicolas N Swainston Neil N Wrzodek Clemens C Wrzodek Clemens C Czauderna Tobias T Keller Roland R Mittag Florian F Schubert Michael M Glont Mihai M Golebiewski Martin M van Iersel Martijn M Keating Sarah S Rall Matthias M Wybrow Michael M Hermjakob Henning H Hucka Michael M Kell Douglas B DB Müller Wolfgang W Mendes Pedro P Zell Andreas A Chaouiya Claudine C Saez-Rodriguez Julio J Schreiber Falk F Laibe Camille C Dräger Andreas A Le Novère Nicolas N

BMC systems biology 20131101

<h4>Background</h4>Systems biology projects and omics technologies have led to a growing number of biochemical pathway models and reconstructions. However, the majority of these models are still created de novo, based on literature mining and the manual processing of pathway data.<h4>Results</h4>To increase the efficiency of model creation, the Path2Models project has automatically generated mathematical models from pathway representations using a suite of freely available software. Data sources ...[more]

PMID: 24180668

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Project description:tRNAs are encoded by a large gene family, usually with several isogenic tRNAs interacting with the same codon. Mutations in the anticodon region of other tRNAs can overcome specific tRNA deficiencies. Phylogenetic analysis suggests that such mutations have occurred in evolution, but the driving force is unclear. We show that in yeast suppressor mutations in other tRNAs are able to overcome deficiency of the essential TRT2-encoded tRNAThrCGU at high temperature (40°C). Surprisingly, these tRNA suppressor mutations were obtained after whole-genome transformation with DNA from thermotolerant Kluyveromyces marxianus or Ogataea polymorpha strains, but from which the mutations did apparently not originate. We suggest that transient presence of donor DNA in the host facilitates proliferation at high temperature and thus increases the chances for occurrence of spontaneous mutations suppressing defective growth at high temperature. Whole-genome sequence analysis of three transformants revealed only four to five non-synonymous mutations of which one causing TRT2 anticodon stem stabilization and two anticodon mutations in non-threonyl-tRNAs, tRNALysCUU and tRNAeMetCAU, were causative. Both anticodon mutations suppressed lethality of TRT2 deletion and apparently caused the respective tRNAs to become novel substrates for threonyl-tRNA synthetase. LC-MS/MS data could not detect any significant mistranslation and RT-qPCR results contradicted induction of the unfolded protein response. We suggest that stress conditions have been a driving force in evolution for the selection of anticodon-switching mutations in tRNAs as revealed by phylogenetic analysis. Importance of the work In this work we have identified for the first time the causative elements in a eukaryotic organism introduced by applying whole-genome transformation and responsible for the selectable trait of interest, i.e. high temperature tolerance. Surprisingly, the whole-genome transformants contained just a few SNPs, which were unrelated to the sequence of the donor DNA. In each of three independent transformants, we have identified a SNP in a tRNA, either stabilizing the essential tRNAThrCGU at high temperature or switching the anticodon of tRNALysCUU or tRNAeMetCAU into CGU, which is apparently enough for in vivo recognition by threonyl-tRNA synthetase. LC-MS/MS analysis indeed indicated absence of significant mistranslation. Phylogenetic analysis showed that similar mutations have occurred throughout evolution and we suggest that stress conditions may have been a driving force for their selection. The low number of SNPs introduced by whole-genome transformation may favor its application for improvement of industrial yeast strains.

Dataset Information

Whole Genome Metabolism - Chlorobaculum parvum (strain NCIB 8327)

Publications

Path2Models: large-scale generation of computational models from biochemical pathway maps.

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